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Crocetin suppresses colorectal cancer progression by targeting TGM2 and inhibiting the JAK2/STAT3 pathway

Shuo Chen1,2, Weijun Su3, Kai Wang4

  • 1Department of Colorectal Surgery, Tianjin Union Medical Center, Tianjin, 300121, China. chenshuo19801106@126.com.

Investigational New Drugs
|March 14, 2026
PubMed
Abstract

Insights

Crocetin, a natural compound, effectively inhibits colorectal cancer (CRC) progression by targeting the TGM2/JAK2/STAT3 pathway. This study identifies TGM2 as a key mediator of crocetin

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Colorectal cancer (CRC) presents a significant health challenge with limited treatment options for advanced stages.
  • Crocetin, a natural compound derived from saffron, exhibits potential anticancer properties, but its precise mechanisms in CRC remain largely unexplored.

Purpose of the Study:

  • To investigate the antitumor effects of crocetin in colorectal cancer.
  • To elucidate the molecular mechanisms underlying crocetin's action in CRC, including identifying its key molecular targets and signaling pathways.

Main Methods:

  • Establishment of a colorectal cancer xenograft mouse model to assess in vivo antitumor efficacy.
  • Transcriptomic analysis to identify differentially expressed genes (DEGs) in response to crocetin treatment.
  • Integration of network pharmacology, protein-protein interaction (PPI) network analysis, and molecular docking to identify potential drug targets.
  • In vitro functional assays (CCK-8, Transwell) to evaluate the impact of crocetin and its target gene, TGM2, on CRC cell behavior.

Main Results:

  • Crocetin significantly suppressed tumor growth in a colorectal cancer xenograft model.
  • Transcriptomic analysis revealed 2,577 differentially expressed genes between crocetin-treated and control groups.
  • Five key target genes (ADAM17, DNMT1, MTOR, TGM2, XRCC6) were identified, all downregulated by crocetin.
  • In vitro studies showed crocetin reduced HCT116 cell viability, migration, and invasion, decreasing TGM2, p-JAK2, and p-STAT3 expression.
  • Overexpression of TGM2 abolished the tumor-suppressive effects of crocetin, highlighting TGM2's critical role.

Conclusions:

  • Crocetin demonstrates significant potential as a therapeutic agent for colorectal cancer.
  • The study elucidates that crocetin suppresses CRC progression by targeting the TGM2/JAK2/STAT3 signaling pathway.
  • TGM2 is identified as a crucial mediator in crocetin's anticancer effects within the TGM2/JAK2/STAT3 pathway.
Keywords:
Colorectal cancerCrocetinJAK2/STAT3 pathwayTGM2Transcriptomics

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